Abstract
Recent studies have revealed synaptic dysfunction to be a hallmark of various psychiatric diseases, and that glial cells participate in synapse formation, development, and plasticity. Glial cells contribute to neuroinflammation and synaptic homeostasis, the latter being essential for maintaining the physiological function of the central nervous system (CNS). In particular, glial cells undergo gliotransmission and regulate neuronal activity in tripartite synapses via ion channels (gap junction hemichannel, volume regulated anion channel, and bestrophin-1), receptors (for neurotransmitters and cytokines), or transporters (GLT-1, GLAST, and GATs) that are expressed on glial cell membranes. In this review, we propose that dysfunction in neuron-glia interactions may contribute to the pathogenesis of neurodevelopmental disorders. Understanding the mechanisms of neuron-glia interaction for synapse formation and maturation will contribute to the development of novel therapeutic targets of neurodevelopmental disorders.
Highlights
Neurodevelopment occurs during the early stages of life
The alteration of neurotransmitters creates an imbalance relative to the normal status. This imbalance could be induced by changes in the expression levels of receptors and transporters, the modification of released gliotransmitters, and through dysfunction of uptake (Figure 3)
As the functions of neurons have been studied extensively previously, it is important to study the role of glial cells in connection with neurons
Summary
Neurodevelopment occurs during the early stages of life. Maturation involves the consolidation of neural wiring, including synapse formation and synapse pruning [1]. Synaptic changes induced by glial cells in the developmental stage, including synaptic patterning secondary to pruning, are being investigated in relation to the neuron-glia interactions [4,5]. In patients with epilepsy, the blood-brain barrier opens, cytokines are known to facilitate functional neurogenesis and induce the release of neurotrophic factors leading to the increased entry of albumin (↑) into the brain and astrocyte activation [16]. MIA induced by the injection of poly I:C in a mother mouse model revealed that P2X7 purinergic receptors drive poly I:C-induced autism-like phenotypes such as social deficits and increased self-grooming [63] This can induce an increase in inflammatory cytokines and impair neurogenesis, resulting in decreased Purkinje cell number and their density in the cerebellum as well as behavioral abnormalities in the fetal brain [101,157].
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